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    Any posts / revision notes / questions...etc. about immunology post here. I would start with a post but i need to revise the topic first.
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    Nope, we're doing it next year. :p:
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    Will be reading up on immunology so will post up some stuff then. Just doing a bit more biochem today.
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    (Original post by nikk)
    Will be reading up on immunology so will post up some stuff then. Just doing a bit more biochem today.
    I should make a start to the thread...

    Hypersensitivities

    Type I (aka. 'immediate hypersensitivity')

    e.g. hayfever

    IgE -> Mast cell activation -> histamine release -> acute inflamatory responce


    Type II

    e.g. Rhesus disease of the newborn

    Foreign blood -> agglutination (formation of IgM and erythrocyte complexes) and compliment activation (lysis of cells)


    Type III (aka. Complex Immunity)

    e.g. glomerulonepherotitis (swelling of the glomerulus and nephrons in the kidney) / arthritis etc.

    Anitgen-antibody complexes (that normally are taken into macrophages) are deposited in tissues and induce the acute inflammatory responce.


    Type IV (aka. delayed hypersensitivity / cell mediated immunity)

    e.g. granuloma formation due to a (mycobacterium) tuberculosis infection


    Type V (secretory hypersensitivity)

    e.g. Grave's disease

    Autoantibody induces hormone production - causing excess thyroid hormone production


    And a quesiton:

    What are the differences between a T and a B cell receptor?
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    There are 2 types of TCR. The TCR on a CD4+ cell recognises MHC Class 2, wheras the TCR on a CD8+ cell recognises an MHC class 1. Both recognise the presented antigens, and bind to the MHC in conjunction with CD4 or CD8. Co-stimulatory molecules such as CD28 are required for full T-cell activation.

    BCRs are simply antibodies embedded in the plasma membrane of a B cell, and bind the antigen directly.
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    (Original post by RichFaut)
    There are 2 types of TCR. The TCR on a CD4+ cell recognises MHC Class 2, wheras the TCR on a CD8+ cell recognises an MHC class 1. Both recognise the presented antigens, and bind to the MHC in conjunction with CD4 or CD8. Co-stimulatory molecules such as CD28 are required for full T-cell activation.

    BCRs are simply antibodies embedded in the plasma membrane of a B cell, and bind the antigen directly.
    Cheers that makes sense...

    Although I don't really understand what you are talking about with T cell activation...
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    (Original post by Revenged)
    Cheers that makes sense...

    Although I don't really understand what you are talking about with T cell activation...
    For a CD8+ T cell to become activated, it must recieve three signals:
    (1) Recognition of MHCI-antigen complex
    (2) Co-stimulatory signal between CD28 on the T cell and B7 ligand on the antigen presenting cell.
    (3) IL-2 - secreted by CD4+ Th1 cells, or if the CD8+ is a memory cell then it can produce its own.

    If any of those three signals are missing then the CD8+ cell will not become activated and hence not react to the antigen.
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    (Original post by nikk)
    For a CD8+ T cell to become activated, it must recieve three signals:
    (1) Recognition of MHCI-antigen complex
    (2) Co-stimulatory signal between CD28 on the T cell and B7 ligand on the antigen presenting cell.
    (3) IL-2 - secreted by CD4+ Th1 cells, or if the CD8+ is a memory cell then it can produce its own.

    If any of those three signals are missing then the CD8+ cell will not become activated and hence not react to the antigen.
    Thanks
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    Yep - and a CD4 recognising an MHC class 2 on a dendritic cell (APC) stimulates it to present an MHC class 1 molecule so that the ctyotoxic CD8 T-cells can recognise the new antigen and proliferate in order to destroy any cells presenting that antigen.

    Can anyone tell me how MHC specificity to antigens works? As in how are the MHCs selected for if there is no antigen present in the cell to start with?

    Also how is the specificity of antibodies produced?
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    (Original post by RichFaut)
    Yep - and a CD4 recognising an MHC class 2 on a dendritic cell (APC) stimulates it to present an MHC class 1 molecule so that the ctyotoxic CD8 T-cells can recognise the new antigen and proliferate in order to destroy any cells presenting that antigen.

    Can anyone tell me how MHC specificity to antigens works? As in how are the MHCs selected for if there is no antigen present in the cell to start with?

    Also how is the specificity of antibodies produced?
    I don't quite understand what you said in the first paragraph....why would a CD4+ cell that recognises antigen with MHC II cause stimulation of MHC I presentation? Surely if a CD4+ recognised MHC II, it would differentiate to a Th2 cell and initiate B cell proliferation instead?

    In answer to your other questions... Cells display both MHCI and MHCII molecules. Which antigens end up being presented with which class of MHC is dependent on the origin of the antigen. If the antigen is present in the cytoplasm (i.e. intracellular bacteria/viruses) then it will be presented with MHCI, but if the antigen was endocytosed/phagocytosed then it will be presented with MHCII. The two paths are quite long to explain - I was going to post them up tomorrow. There is also another pathway for presentation of non-peptide antigens with CD1, but the details of it are not yet known.

    Things are also slightly complicated by 'cross-presentation', the ability of certain APCs to present exogenous antigen with MHCI and endogenous antigen with MHCII.

    As for specifities of antibodies - do you mean how is the diversity of antibodies produced? If so,then that is another (very) long description which I haven't time to explain today. But basically involves a number of gene rearrangements of the genes that encode particular parts of the variable regions of antibodies. Addition of random nucleotides also further increases variation. Following recognition of antigen by a B-cell, 'somatic hypermutation' occurs, a process whereby mutations are caused in the genes encoding the antibodies/BCR of that B-cell, and those B-cells that bind the antigen with an increased affinity are selected for.
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    (Original post by nikk)
    In answer to your other questions... Cells display both MHCI and MHCII molecules. Which antigens end up being presented with which class of MHC is dependent on the origin of the antigen. If the antigen is present in the cytoplasm (i.e. intracellular bacteria/viruses) then it will be presented with MHCI, but if the antigen was endocytosed/phagocytosed then it will be presented with MHCII. The two paths are quite long to explain - I was going to post them up tomorrow. There is also another pathway for presentation of non-peptide antigens with CD1, but the details of it are not yet known.
    Yeh,

    MHC-I -> endogenous pathway -> present in all cells -> if the cell is infected with a virus then viral proteins are taken and put on cell surface membrane -> CD8 T cells recognise this.

    MHC-II -> exogenous pathway -> present on some cells e.g. macrophages -> bacteria is phagocytosed by a macrophage -> bacterial antigen put on the cell membrane -> CD4 T cells recognise this.
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    (Original post by Revenged)
    Yeh,

    MHC-I -> endogenous pathway -> present in all cells -> if the cell is infected with a virus then viral proteins are taken and put on cell surface membrane -> CD8 T cells recognise this.

    MHC-II -> exogenous pathway -> present on some cells e.g. macrophages -> bacteria is phagocytosed by a macrophage -> bacterial antigen put on the cell membrane -> CD4 T cells recognise this.
    As for the endogenous pathway - CD4+ cells also recognise -> differentiate into Th1 cells.
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    (Original post by nikk)
    As for the endogenous pathway - CD4+ cells also recognise -> differentiate into Th1 cells.
    These Th1 cells are involved into macrophage activation in cell mediated immunity




    Edit. I'm been doing some MCQs and quite a few questions...

    1. Activation of C-binding protein occurs during an inflammatory responce - what does the protein do?

    2. Interferon is a major anti-viral agent - but why, what can it do?

    3. Interferon also affects MHC expression - again how?

    4. T cells can help B cells make IgG - but how do T cells cause B cells to change their receptors from IgM and IgD to IgG?
 
 
 
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